Autism: Neural Basis and Treatment Possibilities

Autism: Neural Basis and Treatment Possibilities

Synopsis

This groundbreaking book brings together contributions by leading scientists from different fields to provide a balanced view of the spectrum of current studies on autism. Four main areas of research are covered.Twin and family data indicate that the heritability of the underlying liability to autism exceeds 90%. This probably involves interactions among a relatively small number of susceptibility genes, an hypothesis that is examined in detail.New techniques are now available for examining the neurobiology of autism. The book contains results from imaging studies showing the contributions of different brain regions to this disorder and addresses the neuropathology of autism.There has been considerable discussion in the literature on the fundamental nature of the psychological deficit in children with autism. The book discusses the evidence that so-called 'Theory of mind' deficits are associated with autism.The most important practical question facing medical practitioners is how to help children with autism. Possible psychological or psychiatric interventions for rehabilitation of children with autism are examined in detail. Drug treatments have been disappointing in this field and one chapter addresses this problem.Other topics covered include the epidemiology of autism, immunological aspects_including the possible role of infectious agents in the pathogenesis of neurodevelopmental disorders_and language impairments.This broad-ranging, authoritative book is essential reading for anyone with an interest in autism and its treatment.

Excerpt

There have been many important advances in research into the nature of autism and, as a result, our concepts of autism have undergone a radical change (Rutter 1999). At one time, the prevailing view was that autism was an unusually early variety of schizophrenia that had been caused, in large part, by so-called refrigerator parenting. It became clear that that was a wholly mistaken concept and that, instead, autism constitutes a neurodevelopmental disorder with a rather distinctive pattern of cognitive deficits, and that it is strongly genetically influenced.

Nevertheless, we are a long way from understanding the basic pathophysiology, and numerous puzzles and paradoxes remain. The aim of this symposium is to grapple with these issues, tackling the challenges from a range of different perspectives in the hope that a coming together of minds, and of different research strategies, may point the way ahead. My task is to set the scene by outlining some of these challenges in order to provoke us all to abandon the safety of our own research territory, and of the findings that are well established, in order to focus on the difficulties that are inherent in our favoured theories.

We need to begin with implications of the huge rise in diagnosed autism (Baird et al 2000, Chakrabarti & Fombonne 2001, Fombonne 1999). To a substantial extent, this rise is a consequence of a major broadening of the concept of autism together with better ascertainment. However, is that all? When like is compared with like, has there been a real rise in the rate of autism? If that should prove to be the case, what is the environmental factor that has brought this about (the rise is unlikely to have been genetically determined)? There have been claims that the rise is due to the use of the combined measles/mumps/rubella (MMR) vaccine but that does not seem very likely. The rise began before the introduction of MMR and it continued to rise, without any plateauing, after MMR was used with the vast majority of the population (Dales et al 2001, Farrington et al 2001, Taylor et al 1999). But, if that is not the cause, what is?